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41. Geismann C, Morscheck M, Koch D, Bergmann F, Ungefroren H, Arlt A, Tsao MS, Bachem MG, Altevogt P, Sipos B, Fölsch UR, Schäfer H, Müerköster SS: Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer. Cancer Res; 2009 May 15;69(10):4517-26
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  • [Title] Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer.
  • Pancreatic ductal adenocarcinoma (PDAC) is thought to originate from ductal structures, exhibiting strong desmoplastic reaction with stromal pancreatic myofibroblasts (PMF), which are supposed to drive PDAC tumorigenesis.
  • Thus, this study aimed to investigate whether PMFs are involved in the induction of tumoral L1CAM and whether this contributes to malignant transformation of pancreatic ductal cells and PDAC tumorigenesis.
  • Immunohistochemistry of tissues from chronic pancreatitis specimens revealed considerable L1CAM expression in ductal structures surrounded by dense fibrotic tissue, whereas no L1CAM staining was seen in normal pancreatic tissues.
  • Using the human pancreatic duct cell line H6c7, we show that coculture with PMFs led to a transforming growth factor-beta1 (TGF-beta1)-dependent up-regulation of L1CAM expression.
  • This mechanism of TGF-beta1-induced L1CAM expression and the resulting phenotype could be verified in the TGF-beta1-responsive PDAC cell lines Colo357 and Panc1.
  • Our data provide new insights into the mechanisms of tumoral L1CAM induction and how PMFs contribute to malignant transformation of pancreatic duct cells early in PDAC tumorigenesis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Neural Cell Adhesion Molecule L1 / genetics. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. Cell Line. Cell Line, Tumor. Cell Movement. Cell Transformation, Neoplastic. Coculture Techniques. Humans. Mice. Pancreatitis / pathology. Pancreatitis / surgery. RNA, Small Interfering / genetics. Transfection. Up-Regulation

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  • (PMID = 19435915.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecule L1; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / snail family transcription factors
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42. Pimenova EL, Bogatyrev VN, Chistiakova OV: [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors]. Klin Lab Diagn; 2006 Apr;(4):32-6
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  • [Title] [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors].
  • The study was undertaken to specify cytomorphological criteria for prostatic duct adenocarcinoma (PDAC), by assessing fine-needle aspiration biopsy (FNAB) specimens.
  • For statistical analysis, the authors selected the following cytological signs of malignancy: anisonucleosis, increased nuclei, hyperchromia, uneven chromatin distribution, enucleation, uneven nuclear outline, apocytes; increased nucleoli, nucleolar polymorphism, multiple nucleoli, increased cells, anisocytosis (polymorphism of the size and shape of a cell, mitoses, piled nuclei, papillary structures, slightly glandular structures.
  • [MeSH-major] Adenocarcinoma / diagnosis. Pancreatic Ducts / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16756163.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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43. Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I: The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma. J Pathol; 2009 Oct;219(2):205-13
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  • [Title] The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma.
  • Chronic pancreatitis and pancreatic ductal adenocarcinoma (PDAC) are associated with major changes in cell differentiation.
  • Polycomb proteins are epigenetic silencers expressed in adult stem cells; up-regulation of Polycomb proteins has been reported to occur in a variety of solid tumours such as colon and breast cancer.
  • We hypothesized that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development/progression.
  • To test these ideas, we determined the expression of PRC1 complex proteins (Bmi1 and Ring1b) during pancreatic development and in pancreatic tissue from mouse models of disease: acute and chronic pancreatic injury, duct ligation, and in K-Ras(G12V) conditional knock-in and caerulein-treated K-Ras(G12V) mice.
  • The study was extended to human pancreatic tissue samples.
  • To obtain mechanistic insights, Bmi1 expression in cells undergoing in vitro exocrine cell metaplasia and the effects of Bmi1 depletion in an acinar cancer cell line were studied.
  • We found that Bmi1 and Ring1B are expressed in pancreatic exocrine precursor cells during early development and in ductal and islet cells-but not acinar cells-in the adult pancreas.
  • Bmi1 expression was induced in acinar cells during acute injury, in acinar-ductal metaplastic lesions, as well as in pancreatic intraepithelial neoplasia (PanIN) and PDAC.
  • Our results suggest that Bmi1 and Ring1B are modulated in pancreatic diseases and could contribute differently to tumour development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Nuclear Proteins / metabolism. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cells, Cultured. Disease Models, Animal. Humans. Male. Metaplasia / metabolism. Mice. Mice, Inbred C57BL. Pancreas / metabolism. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Pancreatitis / metabolism. Polycomb Repressive Complex 1. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Wistar. Transcription Factors / metabolism

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  • [Copyright] 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 19585519.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Bmi1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / transcription factor PTF1; EC 6.3.2.19 / Polycomb Repressive Complex 1
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4
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4. Pryczynicz A, Guzińska-Ustymowicz K, Kemona A, Czyzewska J: Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma. Folia Histochem Cytobiol; 2010 Jan 1;48(1):128-33
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  • [Title] Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma.
  • Changes in their expression and functioning reflect invasive and metastatic properties of cancer cells.
  • The study objective was to assess changes in the expressions of E-cadherin and alpha-, beta- and gamma-catenin proteins in pancreatic duct carcinoma in correlation with clinicopathological parameters, lymph node involvement and distant metastases.
  • Twenty-nine patients with pancreatic duct carcinoma were analyzed in relation to gender and age, histological type, histological malignancy grade (G), local lymph node involvement and distant metastases.
  • Reduced expression or abnormal localization of E-cadherin and alpha-, beta- and gamma-catenins were observed in pancreatic duct carcinoma.

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  • (PMID = 20529828.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / CDH1 protein, human; 0 / Cadherins; 0 / Catenins; 0 / alpha Catenin; 0 / beta Catenin; 0 / gamma Catenin
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45. Ji Y, Kuang TT, Tan YS, Chen Y, Zeng HY, Jin DY: Pancreatic primary lymphoma: a case report and review of the literature. Hepatobiliary Pancreat Dis Int; 2005 Nov;4(4):622-6
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  • [Title] Pancreatic primary lymphoma: a case report and review of the literature.
  • BACKGROUND: Primary pancreatic lymphoma is a rare but treatable malignancy (less than 1% of pancreatic tumors) that may be clinically confused with pancreatic adenocarcinoma.
  • METHODS: In a patient with upper abdominal pain, ultrasonography and CT detected a mass in pancreatic head, which compressed the common bile duct.
  • RESULTS: Grossly the tumor involved the pancreatic head, soft in consistence and invaded part of the gastric wall.
  • Histologically, the tumor was composed mainly of large and moderate neoplastic cells, which were diffusely positive for CD20 and Bcl-6 antigens, indicating the features of diffusely large B cell lymphoma.
  • [MeSH-major] Lymphoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 16286277.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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46. Daniel SV, Vani DH, Smith AM, Hill QA, Menon KV: Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult. JOP; 2010;11(1):72-4
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  • [Title] Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult.
  • Liver function tests showed an obstructive picture, full blood count was normal and on computerised tomography there was diffuse enlargement of the pancreas, with dilatation of the common bile duct and intra hepatic biliary radicles.
  • Four weeks after presenting, the white cell count became elevated with blasts on the blood film and bone marrow biopsy revealed a precursor B cell acute lymphoblastic leukaemia.
  • After induction chemotherapy his jaundice resolved, the pancreatic mass reduced in size and he is now in a complete remission.
  • CONCLUSION: Acute lymphoblastic leukaemia may mimic common causes of a pancreatic mass such as adenocarcinoma and should be considered as part of the differential diagnosis when atypical features are present.
  • [MeSH-major] Jaundice, Obstructive / diagnosis. Pancreatic Diseases / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Organ Size. Pancreas / pathology

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  • (PMID = 20065559.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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47. Hayashi A, Aishima S, Miyasaka Y, Nakata K, Morimatsu K, Oda Y, Nagai E, Oda Y, Tanaka M, Tsuneyoshi M: Pdcd4 expression in intraductal papillary mucinous neoplasm of the pancreas: its association with tumor progression and proliferation. Hum Pathol; 2010 Nov;41(11):1507-15
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  • [Title] Pdcd4 expression in intraductal papillary mucinous neoplasm of the pancreas: its association with tumor progression and proliferation.
  • Intraductal papillary mucinous neoplasm is characterized by cystically dilated main and/or branch pancreatic duct with mucus.
  • Programmed cell death 4 is a recently identified tumor suppressor that was found to inhibit translation.
  • Programmed cell death 4 has been reported to inhibit tumorigenesis, tumor progression, proliferation, invasion, and metastasis in several human malignancies.
  • We examined 108 cases of intraductal papillary mucinous neoplasm by immunohistochemistry and revealed that programmed cell death 4 expression was recognized in both the nucleus and cytoplasm in intraductal papillary mucinous neoplasm.
  • The positive rate of programmed cell death 4 was 79%, 43%, and 10% in adenoma, borderline, and carcinoma, respectively.
  • The positive rate of programmed cell death 4 decreased from adenoma to carcinoma (P < .0001, both adenoma versus borderline and borderline versus carcinoma), indicating that programmed cell death 4 might inhibit tumor progression in intraductal papillary mucinous neoplasm.
  • Programmed cell death 4 expression had a strong relationship with p21 expression (P < .0001) and an inverse correlation with Ki-67 labeling index (r = -0.6255, P < .0001).
  • Thus, programmed cell death 4 might inhibit the proliferation of intraductal papillary mucinous neoplasm; and its inhibition might partly result from cell cycle arrest caused by the up-regulation of p21.
  • In conclusion, programmed cell death 4 may inhibit tumor progression in intraductal papillary mucinous neoplasm; and the loss of programmed cell death 4 expression is representative of the malignant potential of intraductal papillary mucinous neoplasm including the proliferative activity.
  • Therefore, programmed cell death 4 can be an important biomarker for intraductal papillary mucinous neoplasm.
  • [MeSH-major] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Papillary / metabolism. Apoptosis Regulatory Proteins / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Ducts / pathology. Pancreatic Neoplasms / metabolism. RNA-Binding Proteins / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / mortality. Adenoma / pathology. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cell Proliferation. Cytoplasm / metabolism. Cytoplasm / pathology. Disease Progression. Fluorescent Antibody Technique, Direct. Humans. Japan / epidemiology. Ki-67 Antigen / metabolism. Survival Rate

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  • [Copyright] Copyright © 2010. Published by Elsevier Inc.
  • (PMID = 20656320.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / PDCD4 protein, human; 0 / RNA-Binding Proteins
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48. Tanno S, Obara T, Koizumi K, Nakano Y, Osanai M, Mizukami Y, Kohgo Y: Risk of additional pancreatic cancer in patients with branch duct intraductal papillary-mucinous neoplasm. Clin J Gastroenterol; 2009 Dec;2(6):365-370
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  • [Title] Risk of additional pancreatic cancer in patients with branch duct intraductal papillary-mucinous neoplasm.
  • Branch duct intraductal papillary-mucinous neoplasms of the pancreas (BD-IPMN) are being diagnosed with increasing frequency.
  • Although BD-IPMN outcomes are generally good, pancreatic ductal adenocarcinoma (PDA) is found distant from the original BD-IPMN in about 3.3-9.2% of cases.
  • Recent findings from follow-up studies suggest that pancreases with BD-IPMNs have a high risk of developing additional pancreatic cancer, with standardized incidence ratios (SIRs) of 15.8- to 26-fold.

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  • (PMID = 26192788.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Branch duct / Follow-up / IPMN / Pancreatic cancer / Risk factor
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49. Logsdon CD, Ji B: Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer. Clin Gastroenterol Hepatol; 2009 Nov;7(11 Suppl):S40-3
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  • [Title] Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.
  • The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear.
  • However, it has been long thought that PDAC arises only from duct cells.
  • However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions.

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  • (PMID = 19896097.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / DK052067
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 46
  • [Other-IDs] NLM/ NIHMS268542; NLM/ PMC3050544
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50. Schneider A, Löhr JM: [Autoimmune pancreatitis]. Internist (Berl); 2009 Mar;50(3):318-30
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  • Morphological hallmarks of the disease are narrowing of the pancreatic duct system and the bile duct by periductal lymphoplasmocytic inflammation.
  • This results in many cases in obstructive jaundice due to a mass-forming lesion in the pancreatic head mimicking pancreatic ductal adenocarcinoma.
  • Autoimmune pancreatitis will respond to steroid treatment, which is of specific importance because pancreatic cancer is one of its clinical differential diagnoses.

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  • (PMID = 19212732.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics
  • [Number-of-references] 133
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51. Hanley S, Rosenberg L: Transforming growth factor beta is a critical regulator of adult human islet plasticity. Mol Endocrinol; 2007 Jun;21(6):1467-77
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  • Tissue plasticity is well documented in the context of pancreatic regeneration and carcinogenesis, with recent reports implicating dedifferentiated islet cells both as endocrine progenitors and as the cell(s) of origin in pancreatic adenocarcinoma.
  • Accordingly, it is noteworthy that accumulating evidence suggests that TGFbeta signaling is essential to pancreatic endocrine development and maintenance, whereas its loss is associated with the progression to pancreatic adenocarcinoma.
  • Human islets were embedded in a collagen gel and cultured under conditions that induced transformation into duct-like epithelial structures (DLS).
  • Localization of TGFbeta signaling molecules suggested that the action of TGFbeta is directly on the beta-cell to inhibit apoptosis and thus stabilize endocrine phenotype.
  • [MeSH-minor] Adult. Cell Differentiation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. MAP Kinase Kinase 4 / metabolism. Pancreatic Ducts / cytology. Pancreatic Ducts / growth & development. Receptors, Transforming Growth Factor beta / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 17405902.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4
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52. Peng SY, Hong DF, Liu YB, Li JT, Tao F, Tan ZJ: [A pancreas suture-less type II binding pancreaticogastrostomy]. Zhonghua Wai Ke Za Zhi; 2009 Dec 1;47(23):1764-6
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  • [Title] [A pancreas suture-less type II binding pancreaticogastrostomy].
  • OBJECTIVE: To explore the feasibility and safety of type II binding pancreaticogastrostomy (BPG) in pancreaticoduodenectomy and mid-segmentectomy of pancreas.
  • METHODS: From November 2008 to May 2009, 26 patients underwent pancreaticoduodenectomy and mid-segmentectomy of pancreas with type II BPG reconstruction, including 13 cases of pancreatic head cancer, 3 cases of duodenal adenocarcinoma, 2 cases of ampullary carcinoma, 4 cases of cholangiocarcinoma, 1 case of bile duct cell severe atypical hyperplasia, and 1 case of stomach cancer.
  • The process of type II BPG was described as the following: after pancreas remnant was mobilized for 2-3 cm, a piece of sero-muscular layer at the posterior gastric wall was excised and then a sero-muscular depth purse-suturing with 3-0 prolene was pre-placed (outer purse-string).
  • Through the two pre-placed purse-strings, the pancreas remnant was pulled into the gastric lumen and then posterior gastric wall was pushed backward to keep it closely in contact with the retro-peritoneal wall.
  • No mortality or pancreatic leakage occurred.
  • CONCLUSIONS: Pancreaticogastrostomy is good for accommodating a large pancreas stump.
  • [MeSH-major] Anastomosis, Surgical / methods. Pancreas / surgery. Stomach / surgery

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  • (PMID = 20193541.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] China
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53. Seeley ES, Carrière C, Goetze T, Longnecker DS, Korc M: Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia. Cancer Res; 2009 Jan 15;69(2):422-30
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  • [Title] Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia.
  • In this study, we determined that ciliogenesis is suppressed in both pancreatic cancer cells and pancreatic intraepithelial neoplasia (PanIN) lesions in human pancreatic ductal adenocarcinoma (PDAC).
  • Inhibition of Kras effector pathways restored ciliogenesis in a mouse pancreatic cancer cell line, raising the possibility that ciliogenesis may be actively repressed by oncogenic Kras.
  • By contrast, normal duct, islet, and centroacinar cells retained primary cilia in both human and mouse pancreata.

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  • (PMID = 19147554.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102687-05; United States / NCI NIH HHS / CA / CA-102687; United States / NCI NIH HHS / CA / R01 CA102687; United States / NCI NIH HHS / CA / CA-127095; United States / NCI NIH HHS / CA / R01 CA102687-05; United States / NCI NIH HHS / CA / CA-101306; United States / NCI NIH HHS / CA / R21 CA127095; United States / NCI NIH HHS / CA / R01 CA075059; United States / NCI NIH HHS / CA / CA101306-05; United States / NCI NIH HHS / CA / R01 CA101306; United States / NCI NIH HHS / CA / R01 CA101306-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS79339; NLM/ PMC2629528
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54. Shimizu K, Kitahashi T, Fujii H, Tsutsumi M, Mori T, Honoki K, Tsujiuchi T: Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines. Oncol Rep; 2006 Jul;16(1):85-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines.
  • Alterations of the Smad4 gene, identified as a mediator of the transforming growth factor-beta pathway, were investigated in hamster pancreatic duct adenocarcinomas (PDAs) and established cell lines.
  • A total of 12 PDAs obtained 10 weeks after beginning the experiment and three cell lines established from subcutaneously transplantable PDAs in syngeneic hamsters were examined for mutations using reverse transcription-polymerase chain reaction-single strand conformation polymorphism (RT-PCR-SSCP) analysis.
  • A mutation was detected in only one PDA (1/12, 8.3%) in the form of an ACC to ATC (Thr to IIe) transition at codon 73; none were detected in the three cell lines.
  • These results suggest that the Smad4 gene might play a role in limited fraction of BOP-induced pancreatic duct carcinogenesis in hamsters.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Gene Expression Regulation, Neoplastic. Smad4 Protein / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cricetinae. Female. Genetic Predisposition to Disease. Mesocricetus. Nitrosamines. Polymorphism, Single-Stranded Conformational. RNA / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16786127.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Nitrosamines; 0 / Smad4 Protein; 60599-38-4 / nitrosobis(2-oxopropyl)amine; 63231-63-0 / RNA
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55. Nielsen SK, Møllgård K, Clement CA, Veland IR, Awan A, Yoder BK, Novak I, Christensen ST: Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines. Dev Dyn; 2008 Aug;237(8):2039-52
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  • [Title] Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines.
  • Hedgehog (Hh) signaling controls pancreatic development and homeostasis; aberrant Hh signaling is associated with several pancreatic diseases.
  • Here we investigated the link between Hh signaling and primary cilia in the human developing pancreatic ducts and in cultures of human pancreatic duct adenocarcinoma cell lines, PANC-1 and CFPAC-1.
  • We show that the onset of Hh signaling from human embryogenesis to fetal development is associated with accumulation of Hh signaling components Smo and Gli2 in duct primary cilia and a reduction of Gli3 in the duct epithelium.
  • These findings indicate that primary cilia are involved in pancreatic development and postnatal tissue homeostasis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Cilia / metabolism. Hedgehog Proteins / metabolism. Pancreas / cytology. Pancreas / embryology. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Epithelial Cells / metabolism. Epithelial Cells / ultrastructure. Female. Fetus / cytology. Green Fluorescent Proteins / genetics. Humans. Kruppel-Like Transcription Factors / genetics. Kruppel-Like Transcription Factors / metabolism. Mice. NIH 3T3 Cells. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Pregnancy. Receptors, Cell Surface / metabolism. Receptors, G-Protein-Coupled. Transfection

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  • [Copyright] Copyright (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18629868.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 R01-HD056030
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI2 protein, human; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Nuclear Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / SHH protein, human; 0 / SMO protein, human; 0 / patched receptors; 147336-22-9 / Green Fluorescent Proteins
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56. Radulovich N, Pham NA, Strumpf D, Leung L, Xie W, Jurisica I, Tsao MS: Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma. Mol Cancer; 2010 Feb 01;9:24
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  • [Title] Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma.
  • BACKGROUND: The cyclin D1 (CCND1) and cyclin D3 (CCND3) are frequently co-overexpressed in pancreatic ductal adenocarcinoma (PDAC).
  • RESULTS: CCND1 and CCND3 expression were selectively suppressed by shRNA in PDAC cell lines with expression levels of equal CCND1 and CCND3 (BxPC3), enhanced CCND1 (HPAC) or enhanced CCND3 (PANC1).
  • Suppression of cell proliferation was greater with CCND3 than CCND1 downregulation.
  • The downregulated gene targets in CCND3 suppressed cells were significantly enriched in cell cycle associated processes (p < 0.005).
  • CONCLUSIONS: Our results suggest that CCND3 is the primary driver of the cell cycle, in cooperation with CCND1 that integrates extracellular mitogenic signaling.
  • We also present evidence that CCND1 plays a role in tumor cell migration.
  • The results provide novel insights for common and differential targets of CCND1 and CCND3 overexpression during pancreatic duct cell carcinogenesis.

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  • (PMID = 20113529.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-49585
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / CCND1 protein, human; 0 / CCND3 protein, human; 0 / Cyclin D3; 136601-57-5 / Cyclin D1; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2824633
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57. Sugita H, Hirota M, Ichihara A, Furuhashi S, Kihara S, Shimada S: Combined chemotherapy of irinotecan and low-dose cisplatin (I/low-P) against metastatic biliary tract cancer. J Hepatobiliary Pancreat Surg; 2006;13(5):463-7
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  • [Title] Combined chemotherapy of irinotecan and low-dose cisplatin (I/low-P) against metastatic biliary tract cancer.
  • There is no established or effective standard therapy for metastatic biliary tract cancer, resulting in poor prognosis.
  • Recently, we performed combination chemotherapy of irinotecan and low-dose cisplatin (I/low-P) for three consecutive patients with metastatic biliary tract cancer.
  • These outcomes suggest that I/low-P therapy is safe and may be worth trying as a first-line chemotherapy for patients with metastatic biliary tract cancer.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Bile Duct Neoplasms / drug therapy. Bile Duct Neoplasms / pathology. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Cisplatin / administration & dosage. Female. Gallbladder Neoplasms / drug therapy. Gallbladder Neoplasms / pathology. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 17013724.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 7673326042 / irinotecan; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
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58. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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59. Schuller HM, Al-Wadei HA, Majidi M: GABA B receptor is a novel drug target for pancreatic cancer. Cancer; 2008 Feb 15;112(4):767-78
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  • [Title] GABA B receptor is a novel drug target for pancreatic cancer.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death.
  • It has been shown that the growth of PDAC and pancreatic duct epithelial cells is regulated by beta-adrenoreceptors (beta-ARs).
  • The aim of the study was to investigate if GABA B R inhibits beta-AR signaling in PDAC and pancreatic duct epithelial cells, thus blocking driving forces of cancer progression, such as cell proliferation and cell migration.
  • METHODS: Intracellular cAMP was measured by immunoassays, DNA synthesis by BrdU incorporation assays, activation of ERK1/2 by ERK activation assays, and Western blots and metastatic potential by cell migration assays in the human PDAC cell lines PANC-1 and BXPC-3 and immortalized human pancreatic duct epithelial cells HPDE6-C7.
  • DNA synthesis and cell migration were stimulated by isoproterenol, responses blocked by GABA and baclofen.
  • CONCLUSIONS: The data suggest the stimulation of GABA B R signaling as a novel target for the treatment and prevention of pancreatic cancer.

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  • [Copyright] Cancer 2008. (c) 2007 American Cancer Society.
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  • (PMID = 18098271.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829; United States / NCI NIH HHS / CA / R01 CA42829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / GABA Agents; 0 / GABA Agonists; 0 / Receptors, GABA; 56-12-2 / gamma-Aminobutyric Acid; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; G34N38R2N1 / Bromodeoxyuridine; H789N3FKE8 / Baclofen; L628TT009W / Isoproterenol
  • [Other-IDs] NLM/ NIHMS381601; NLM/ PMC3375598
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60. Brune K, Abe T, Canto M, O'Malley L, Klein AP, Maitra A, Volkan Adsay N, Fishman EK, Cameron JL, Yeo CJ, Kern SE, Goggins M, Hruban RH: Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer. Am J Surg Pathol; 2006 Sep;30(9):1067-76
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  • [Title] Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer.
  • We screened 116 patients with a strong family history of pancreatic cancer using a combination of endoscopic ultrasound and computed tomography.
  • Ten of these patients underwent surgical resection at our institution, providing an opportunity to define the morphology of pancreatic precursor lesions in patients with a strong family history of pancreatic cancer.
  • The number of pancreatic intraepithelial neoplasia (PanIN) lesions and intraductal papillary mucinous neoplasms (IPMNs) were compared with age-matched controls.
  • PanINs were significantly more common in the 8 cases (mean of 10.7% of the duct profiles, range 1.0% to 27.3%) than in the controls (mean 1.9%, range 0% to 9.2%, P<0.01).
  • Some individuals with a strong family history of pancreatic cancer develop multifocal, noninvasive epithelial precursor lesions of the pancreas.
  • The multifocal nature of familial pancreatic neoplasia suggests that surveillance of these patients is warranted after partial pancreatectomy.

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  • (PMID = 16931950.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-140011; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-120011; United States / NCI NIH HHS / CA / P50 CA062924-130011; United States / NCI NIH HHS / CA / P50 CA062924-120011; United States / NCI NIH HHS / CA / R01 CA97075; United States / NCI NIH HHS / CA / R01 CA097075; United States / NCI NIH HHS / CA / CA062924-130011; United States / NCI NIH HHS / CA / CA062924-140011
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS105552; NLM/ PMC2746409
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61. Hsu HP, Shan YS, Lai MD, Lin PW: Osteopontin-positive infiltrating tumor-associated macrophages in bulky ampullary cancer predict survival. Cancer Biol Ther; 2010 Jul 15;10(2):144-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteopontin-positive infiltrating tumor-associated macrophages in bulky ampullary cancer predict survival.
  • PURPOSE: Tumor-associated macrophages (TAMs) promote cancer cell proliferation and distant metastases.
  • Osteopontin (OPN) is overexpressed in several human cancer cells and in TAMs.
  • Therefore, we set out to determine the role of OPN-expressing macrophages in cancer.
  • Expression patterns of OPN in TAMs were associated with pancreatic invasion, tumor stage, TNM stage, lymphovascular invasion and recurrence with peritoneal carcinomatosis.
  • Macrophage-associated cytokine expression in ampullary cancer cells was also assessed; levels of macrophage migration inhibitory factor (MIF) in cancer cells were higher than in normal duodenal mucosa.
  • EXPERIMENTAL DESIGN: Specimens from ampullary cancer patients at National Cheng Kung University Hospital were collected for immunohistochemistry.
  • CONCLUSIONS: Expression of OPN and location of TAMs in bulky ampullary cancer predict recurrence.
  • In addition, cytoplasmic staining of MIF is enhanced in ampullary cancer cells.
  • [MeSH-major] Adenocarcinoma / pathology. Ampulla of Vater / pathology. Biomarkers, Tumor / metabolism. Common Bile Duct Neoplasms / pathology. Macrophage Migration-Inhibitory Factors / metabolism. Macrophages / metabolism. Osteopontin / metabolism. RNA, Neoplasm / metabolism

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  • (PMID = 20495367.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Macrophage Migration-Inhibitory Factors; 0 / RNA, Neoplasm; 106441-73-0 / Osteopontin
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62. Zhang L, Notohara K, Levy MJ, Chari ST, Smyrk TC: IgG4-positive plasma cell infiltration in the diagnosis of autoimmune pancreatitis. Mod Pathol; 2007 Jan;20(1):23-8
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  • [Title] IgG4-positive plasma cell infiltration in the diagnosis of autoimmune pancreatitis.
  • Autoimmune pancreatitis typically produces an enlarged pancreas with narrowing of the pancreatic duct, and can mimic carcinoma.
  • Autoimmune pancreatitis usually responds to corticosteroid treatment, making it important to differentiate from pancreatic ductal adenocarcinoma.
  • We investigated the role of IgG4 staining in the diagnosis of autoimmune pancreatitis, first in resected pancreas specimens (29 autoimmune pancreatitis, nine chronic alcoholic pancreatitis and 25 pancreatic cancer), then in pancreatic needle biopsies.
  • When we subdivided autoimmune pancreatitis into the histologic subtypes lymphoplasmacytic sclerosing pancreatitis and idiopathic duct-destructive pancreatitis, 16/17 lymphoplasmacytic sclerosing pancreatitis had moderate to marked staining, compared to five to 12 idiopathic duct-destructive pancreatitis.
  • We conclude that pancreatic tissue from patients with autoimmune pancreatitis often shows moderate or marked infiltration by IgG4-positive plasma cells (>10/HPF).
  • We rarely see IgG4 staining in patients with chronic alcoholic pancreatitis and pancreatic ductal adenocarcinoma.
  • [MeSH-minor] Adenocarcinoma / immunology. Adenocarcinoma / pathology. Adolescent. Aged. Biomarkers / analysis. Carcinoma, Pancreatic Ductal / immunology. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / pathology. Pancreatitis, Alcoholic / immunology. Pancreatitis, Alcoholic / pathology. Severity of Illness Index

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  • (PMID = 16980948.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Immunoglobulin G
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63. Chu PG, Schwarz RE, Lau SK, Yen Y, Weiss LM: Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2. Am J Surg Pathol; 2005 Mar;29(3):359-67
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  • [Title] Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2.
  • We studied the expression of cytokeratin 7 (CK7), cytokeratin 17 (CK17), cytokeratin 20 (CK20), CDX2, mucin 1 (MUC1), mucin 2 (MUC2), and mucin 5AC (MUC5AC) in 46 cases of pancreatic ductal carcinoma, 18 ampulla of Vater adenocarcinomas, and 24 intrahepatic cholangiocarcinomas.
  • The expression of MUC1 and CK17 was restricted to pancreatic ductal carcinoma (41 of 46, 89%; 38 of 46, 83%, respectively), the ampullary carcinoma of pancreatobiliary origin (6 of 6, 100%; 5 of 6, 83%, respectively), and intrahepatic cholangiocarcinoma (20 of 24, 83%; 17 of 24, 71%, respectively).
  • The expression of MUC2 and CDX2 was restricted to the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin (9 of 11, 82%; 11 of 11, 100%, respectively).
  • MUC2 was rarely expressed in pancreatic ductal carcinoma (1 of 46, 2%) and was negative in the ampullary carcinoma of pancreatobiliary origin and in intrahepatic cholangiocarcinoma.
  • A heterogeneous CDX2 staining pattern was seen in 1 of 6 cases of the ampullary carcinoma of pancreatobiliary origin (17%), 5 of 24 intrahepatic cholangiocarcinomas (21%), and 10 of 46 (22%) pancreatic ductal carcinomas.
  • In contrast, all 11 cases of the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin showed homogeneous CDX2 nuclear positivity.
  • MUC1+/CK17+ can be used as positive markers for pancreatic ductal carcinomas, the ampullary carcinoma of pancreatobiliary origin, and cholangiocarcinomas with positive predictive values of 76%, 83%, and 58%, respectively.
  • MUC2+/CDX2+ can be used as positive markers for the intestinal-type adenocarcinoma of duodenal papillary origin with a positive predictive value of 82%.
  • [MeSH-major] Ampulla of Vater / pathology. Bile Ducts, Intrahepatic / pathology. Carcinoma, Pancreatic Ductal / pathology. Cholangiocarcinoma / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratins / metabolism. Male. Mucins / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 15725805.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Mucins; 0 / Neoplasm Proteins; 68238-35-7 / Keratins
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64. Kelly KA, Bardeesy N, Anbazhagan R, Gurumurthy S, Berger J, Alencar H, Depinho RA, Mahmood U, Weissleder R: Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma. PLoS Med; 2008 Apr 15;5(4):e85
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  • [Title] Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, typically presenting with metastasis at the time of diagnosis and exhibiting profound resistance to existing therapies.
  • METHODS AND FINDINGS: Here, a phage display approach was used in a mouse model of PDAC to screen for peptides that specifically bind to cell surface antigens on PDAC cells.
  • These screens yielded a motif that distinguishes PDAC cells from normal pancreatic duct cells in vitro, which, upon proteomics analysis, identified plectin-1 as a novel biomarker of PDAC.

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  • (PMID = 18416599.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA086355; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / K01 CA104647-03; United States / NCI NIH HHS / CA / P50-CA86355; United States / NCI NIH HHS / CA / P01-CA117969-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Plec protein, mouse; 0 / Plectin
  • [Other-IDs] NLM/ PMC2292750
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65. Corbo V, Ritelli R, Barbi S, Funel N, Campani D, Bardelli A, Scarpa A: Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas. PLoS One; 2010;5(9):e12653
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  • [Title] Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas.
  • Tumours of the pancreas are aggressive neoplasms for which no effective therapeutic strategy is currently available.
  • METHODOLOGY/PRINCIPAL FINDINGS: We conducted a DNA-sequence analysis of a selected set of 35 kinase genes in a panel of 52 pancreatic exocrine neoplasms, including 36 pancreatic ductal adenocarcinoma, and 16 ampulla of Vater cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Common Bile Duct Neoplasms / genetics. Mutation. Pancreatic Neoplasms / genetics. Protein Kinases / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ampulla of Vater / enzymology. Base Sequence. Cell Line, Tumor. Female. Humans. Male. Middle Aged. Molecular Sequence Data


66. Radulovich N, Qian JY, Tsao MS: Human pancreatic duct epithelial cell model for KRAS transformation. Methods Enzymol; 2008;439:1-13
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  • [Title] Human pancreatic duct epithelial cell model for KRAS transformation.
  • Mutations on the KRAS gene occur early during pancreatic duct cell carcinogenesis and have been identified in up to 90% of ductal adenocarcinoma.
  • However, the functional role of KRAS mutations in the malignant transformation of normal pancreatic duct epithelial cells into cancer cells remains unknown.
  • We have developed an in vitro model for KRAS transformation using near-normal HPV-16E6E7-immortalized human pancreatic ductal epithelial (HPDE-E6E7) cells.
  • The model provides an opportunity to dissect further the molecular and cellular mechanisms associated with human pancreatic duct cell carcinogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Pancreatic Ducts / cytology. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. ras Proteins / genetics. ras Proteins / physiology
  • [MeSH-minor] Cell Culture Techniques / methods. Epithelial Cells / physiology. Genes, ras / physiology. Humans

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  • (PMID = 18374152.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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67. De La O JP, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC: Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18907-12
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  • [Title] Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
  • Efforts to model pancreatic cancer in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations that occur in pancreatic tumors and their putative precursors, pancreatic intraepithelial neoplasia (PanIN).
  • The basis for this selective response is unknown, and it is similarly unknown what cell types in the mature pancreas actually contribute to PanINs.
  • One clue comes from the fact that PanINs, unlike most cells in the adult pancreas, exhibit active Notch signaling.
  • We hypothesize that Notch, which inhibits differentiation in the embryonic pancreas, contributes to PanIN formation by abrogating the normal differentiation program of tumor-initiating cells.
  • Through conditional expression in the mouse pancreas, we find dramatic synergy between activated Notch and Kras in inducing PanIN formation.
  • Furthermore, we find that Kras activation in mature acinar cells induces PanIN lesions identical to those seen upon ubiquitous Kras activation, and that Notch promotes both initiation and dysplastic progression of these acinar-derived PanINs, albeit short of invasive adenocarcinoma.
  • At the cellular level, Notch/Kras coactivation promotes rapid reprogramming of acinar cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor can arise from nonductal acinar cells.

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  • (PMID = 19028876.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / CA123066-02; United States / NCI NIH HHS / CA / R21 CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NCI NIH HHS / CA / P30 CA042014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 094ZI81Y45 / Tamoxifen; EC 3.6.5.2 / ras Proteins
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68. Grützmann R, Niedergethmann M, Pilarsky C, Klöppel G, Saeger HD: Intraductal papillary mucinous tumors of the pancreas: biology, diagnosis, and treatment. Oncologist; 2010;15(12):1294-309
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  • [Title] Intraductal papillary mucinous tumors of the pancreas: biology, diagnosis, and treatment.
  • Pancreatic intraductal papillary mucinous neoplasms (IPMNs) rank among the most common cystic tumors of the pancreas.
  • For a long time they were misdiagnosed as mucinous cystadenocarcinoma, ductal adenocarcinoma in situ, or chronic pancreatitis.
  • There are main duct and branch duct IPMNs, with the main duct type including the intestinal, pancreatobiliary, and oncocytic types and the branch duct type solely harboring the gastric type.
  • Whereas main duct IPMNs have a high risk for malignant progression, demanding their resection, branch duct IPMNs have a much lower risk for harboring malignancy.
  • Patients with small branch duct/gastric-type IPMNs (<2 cm) without symptoms or mural nodules can be managed by periodic surveillance.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adenocarcinoma, Mucinous / diagnosis. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / therapy. Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / therapy. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / therapy. Humans. Prognosis

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  • (PMID = 21147870.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3227924
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69. Prenzel KL, Warnecke-Eberz U, Brabender J, Baldus SE, Bollschweiler E, Gutschow CA, Drebber U, Hoelscher AH, Schneider PM: Differential c-erbB-1 and c-erbB-2 mRNA expression in cancer of the pancreas compared with cancer of the papilla of Vater. World J Gastroenterol; 2006 Jan 21;12(3):437-42
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  • [Title] Differential c-erbB-1 and c-erbB-2 mRNA expression in cancer of the pancreas compared with cancer of the papilla of Vater.
  • AIM: We examined quantitative mRNA expression of growth factor receptors (c-erbB-1, c-erbB-2) and the anti-apoptosis gene survivin known to be regulated in pancreatic adenocarcinomas and compared the expression pattern with that in carcinomas of the papilla of Vater.
  • METHODS: Quantitative real-time reverse transcriptase-PCR (QRT-PCR, Taqman) was performed to analyze mRNA expression levels of c-erbB-1, c-erbB-2 and survivin in normal and corresponding tumor samples of 31 pancreatic adenocarcinomas and 8 cancers of the papilla of Vater.
  • RESULTS: The overall median mRNA expression of survivin was significantly increased in both adenocarcinoma of the pancreas (P<0.01) and papilla of Vater (P<0.008) compared with uninvolved normal control tissue.
  • In pancreatic cancer, expression of c-erbB-1 was significantly decreased compared with the normal pancreatic tissue (P<0.03), whereas in the cancer of the papilla of Vater expression of c-erbB-2 was significantly downregulated (P<0.05) compared with the paired normal samples.
  • CONCLUSION: The common anti-apoptosis gene survivin is overexpressed both in the cancer of the papilla of Vater and pancreas.
  • In contrast, the growth factor receptor genes c-erbB-1 and c-erbB-2 are differentially regulated in both tumor entities adding further evidence that pancreatic cancer is biologically different from the cancer of papilla of Vater.
  • [MeSH-major] Adenocarcinoma / metabolism. Ampulla of Vater. Common Bile Duct Neoplasms / metabolism. Pancreatic Neoplasms / metabolism. RNA, Messenger / genetics. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism

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  • (PMID = 16489645.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC4066064
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70. Lisovsky M, Dresser K, Woda B, Mino-Kenudson M: Immunohistochemistry for cell polarity protein lethal giant larvae 2 differentiates pancreatic intraepithelial neoplasia-3 and ductal adenocarcinoma of the pancreas from lower-grade pancreatic intraepithelial neoplasias. Hum Pathol; 2010 Jun;41(6):902-9
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  • [Title] Immunohistochemistry for cell polarity protein lethal giant larvae 2 differentiates pancreatic intraepithelial neoplasia-3 and ductal adenocarcinoma of the pancreas from lower-grade pancreatic intraepithelial neoplasias.
  • Pancreatic intraepithelial neoplasia is a precursor to ductal adenocarcinoma of the pancreas that shows gastric differentiation.
  • Pancreatic intraepithelial neoplasia-3 has the highest potential to progress to adenocarcinoma, and its distinction from lower-grade pancreatic intraepithelial neoplasias is important for clinical management.
  • However, morphologic grading of pancreatic intraepithelial neoplasia suffers from significant interobserver variability.
  • A product of cell polarity gene lethal giant larvae 2 is a marker of gastric foveolar epithelium expressed in a basolateral fashion, which is lost or mislocalized in gastric epithelial dysplasia and adenocarcinoma.
  • In this study, we investigated a role of lethal giant larvae 2 expression in differentiating low-grade pancreatic intraepithelial neoplasias, that is, pancreatic intraepithelial neoplasia-1 and pancreatic intraepithelial neoplasia-2, from pancreatic intraepithelial neoplasia-3 and pancreatic ductal adenocarcinoma.
  • The immunohistochemical patterns of lethal giant larvae 2 expression were examined in normal pancreatic ducts, 48 pancreatic intraepithelial neoplasia lesions of all histologic grades, and 91 adenocarcinomas on a tissue microarray or conventional sections.
  • Whereas normal duct epithelia did not exhibit lethal giant larvae immunoreactivity, all but one lesion of low-grade pancreatic intraepithelial neoplasia showed basolateral lethal giant larvae staining.
  • Conversely, all lesions of pancreatic intraepithelial neoplasia-3 and adenocarcinoma showed loss of lethal giant larvae 2 staining and/or its cytoplasmic localization.
  • In conclusion, our results show that low-grade pancreatic intraepithelial neoplasias express lethal giant larvae 2 in a basolateral fashion recapitulating expression in normal gastric epithelium.
  • Loss or abnormal lethal giant larvae 2 expression is seen in pancreatic intraepithelial neoplasia-3 and adenocarcinoma and might be useful in separating them from lower-grade pancreatic intraepithelial neoplasias.
  • [MeSH-major] Carcinoma in Situ / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Cytoskeletal Proteins / biosynthesis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Cell Polarity. Diagnosis, Differential. Gastric Mucosa / metabolism. Humans. Immunohistochemistry. Pancreas / metabolism. Pancreas / pathology

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20233622.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
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71. Sano T, Shimada K, Sakamoto Y, Ojima H, Esaki M, Kosuge T: Prognosis of perihilar cholangiocarcinoma: hilar bile duct cancer versus intrahepatic cholangiocarcinoma involving the hepatic hilus. Ann Surg Oncol; 2008 Feb;15(2):590-9
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  • [Title] Prognosis of perihilar cholangiocarcinoma: hilar bile duct cancer versus intrahepatic cholangiocarcinoma involving the hepatic hilus.
  • BACKGROUND: Clinically hepatobiliary resection is indicated for both hilar bile duct cancer (BDC) and intrahepatic cholangiocarcinoma involving the hepatic hilus (CCC).
  • On multivariate analysis, three independent factors were related to longer survival in BDC patients: achieved in curative resection with cancer free margin (R0) (P = .024, odds ratio 1.862), well differentiated or papillary adenocarcinoma (P = .011, odds ratio 2.135), and absence of lymph node metastasis (P < .001, odds ratio 3.314).
  • Five factors were related to longer survival in CCC patients: absence of intrahepatic daughter nodules (P < .001, odds ratio 2.318), CEA level </=2.9 ng/mL (P = .005, odds ratio 2.606), no red blood cell transfusion requirement (P = .016, odds ratio 2.614), absence or slight degree of lymphatic system invasion (P < .001, odds ratio 4.577), and negative margin of the proximal bile duct (P = .003, odds ratio 7.398).
  • [MeSH-major] Bile Duct Neoplasms / mortality. Bile Ducts, Intrahepatic. Cholangiocarcinoma / mortality
  • [MeSH-minor] Adult. Cell Differentiation. Female. Hepatectomy. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local / mortality. Prognosis. Proportional Hazards Models. Risk Factors. Survival Analysis

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  • (PMID = 18057991.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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72. Verbeke CS, Menon KV: Osteoclast-like giant cell tumour of the pancreas: an undifferentiated carcinoma of duct epithelial origin. Pancreatology; 2006;6(3):254; author reply 254
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  • [Title] Osteoclast-like giant cell tumour of the pancreas: an undifferentiated carcinoma of duct epithelial origin.
  • [MeSH-major] Adenocarcinoma / therapy. Giant Cell Tumors / therapy. Pancreatic Neoplasms / therapy

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  • [CommentOn] Pancreatology. 2005;5(2-3):279-84 [15849490.001]
  • (PMID = 16534249.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] Switzerland
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73. Katayama M, Funakoshi A, Sumii T, Sanzen N, Sekiguchi K: Laminin gamma2-chain fragment circulating level increases in patients with metastatic pancreatic ductal cell adenocarcinomas. Cancer Lett; 2005 Jul 8;225(1):167-76
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  • [Title] Laminin gamma2-chain fragment circulating level increases in patients with metastatic pancreatic ductal cell adenocarcinomas.
  • Laminin-5 (LN5) is expressed solely by epithelial cells and considered to enhance cell migration after being cleaved by proteases, leading to the shedding of the N-terminal fragment of the LN5 gamma2-chain (G2F).
  • The G2F level in pancreatic ductal cell adenocarcinoma patients with liver metastases was markedly elevated, but that in patients without liver metastases was not significantly elevated.
  • The G2F levels in patients with benign pancreatic tumours (pancreatic cysts and intraductal papillary mucinous tumours) were similar to that in healthy volunteers.
  • Interestingly, a significant increase in circulating G2F/G1F ratio was observed in patients with bile duct and gallbladder carcinoma, as well as in those with metastatic pancreatic ductal cell adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Cell Adhesion Molecules / blood. Laminin / blood. Liver Neoplasms / secondary. Neoplasm Metastasis. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology

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  • (PMID = 15922869.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / LAMC2 protein, human; 0 / Laminin; 0 / kalinin
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74. Bloomston M, Chanona-Vilchis J, Ellison EC, Ramirez NC, Frankel WL: Carcinosarcoma of the pancreas arising in a mucinous cystic neoplasm. Am Surg; 2006 Apr;72(4):351-5
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  • [Title] Carcinosarcoma of the pancreas arising in a mucinous cystic neoplasm.
  • We report a carcinosarcoma of the pancreas in a 67-year-old woman who presented with nausea, vomiting, and painless jaundice.
  • A work-up demonstrated a well-circumscribed mass in the head of the pancreas.
  • After pylorus-preserving pancreaticoduodenectomy, the tumor was found to be grossly yellow, and it compressed the common bile duct and pancreatic duct.
  • Histological examination of the neoplasm showed a 4.0 x 4.0 x 3.0-cm mucinous cystadenocarcinoma with invasive poorly differentiated carcinoma, well-differentiated squamous cell carcinoma, and sarcomatous stroma invading into the duodenum.
  • To the best of our knowledge, this is the second case of carcinosarcoma with invasive epithelial and sarcomatous areas in the background of a mucinous cystic neoplasm of the pancreas.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinosarcoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 16676863.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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75. Salla C, Chatzipantelis P, Konstantinou P, Karoumpalis I, Pantazopoulou A, Dappola V: Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid pseudopapillary tumor of the pancreas: a case report and literature review. World J Gastroenterol; 2007 Oct 14;13(38):5158-63
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  • [Title] Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid pseudopapillary tumor of the pancreas: a case report and literature review.
  • We describe the clinical, imaging and cytopathological features of solid pseudopapillary tumor of the pancreas (SPTP) diagnosed by endoscopic ultrasound-guided (EUS-guided) fine-needle aspiration (FNA).
  • Computed tomography (CT) analysis revealed a mass of the pancreatic tail with solid and cystic consistency.
  • EUS confirmed the mass, both in body and tail of the pancreas, with distinct borders, which caused dilation of the peripheral part of the pancreatic duct (major diameter 3.7 mm).
  • EUS findings, cytomorphologic features and immunostains of cell block help distinguish SPTP from pancreatic endocrine tumors, acinar cell carcinoma and papillary mucinous carcinoma.
  • [MeSH-major] Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Mucinous / diagnosis. Adenocarcinoma, Mucinous / pathology. Adolescent. Biopsy, Fine-Needle / methods. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Diagnosis, Differential. Endosonography / methods. Female. Humans. Pancreas / pathology. Pancreas / ultrasonography

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  • (PMID = 17876886.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 59
  • [Other-IDs] NLM/ PMC4434650
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76. Nakakura EK, Bergsland EK: Islet cell carcinoma: neuroendocrine tumors of the pancreas and periampullary region. Hematol Oncol Clin North Am; 2007 Jun;21(3):457-73; viii
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  • [Title] Islet cell carcinoma: neuroendocrine tumors of the pancreas and periampullary region.
  • Most patients who have islet cell tumors, except those who have insulinomas, present with locally advanced or metastatic disease.
  • In contrast with patients who have adenocarcinoma of the pancreas, those who have islet cell carcinomas can achieve long-term survival even if their disease is advanced.
  • [MeSH-major] Carcinoma, Islet Cell. Common Bile Duct Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms

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  • (PMID = 17548034.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 57
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77. Alldinger I, Dittert D, Peiper M, Fusco A, Chiappetta G, Staub E, Lohr M, Jesnowski R, Baretton G, Ockert D, Saeger HD, Grützmann R, Pilarsky C: Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer. Pancreatology; 2005;5(4-5):370-9
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  • [Title] Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer.
  • BACKGROUND: Pancreatic cancer is one of the leading causes of cancer-related death.
  • Using DNA gene expression analysis based on a custom made Affymetrix cancer array, we investigated the expression pattern of both primary and established pancreatic carcinoma cell lines.
  • METHODS: We analyzed the gene expression of 5 established pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-1, Capan-2 and HPAF II) and 5 primary isolates, 1 of them derived from benign pancreatic duct cells.
  • RESULTS: Out of 1,540 genes which were expressed in at least 3 experiments, we found 122 genes upregulated and 18 downregulated in tumor cell lines compared to benign cells with a fold change >3.
  • Several of the upregulated genes (like Prefoldin 5, ADAM9 and E-cadherin) have been associated with pancreatic cancer before.
  • The other differentially regulated genes, however, play a so far unknown role in the course of human pancreatic carcinoma.
  • By means of immunohistochemistry we could show that thymosin beta-10 (TMSB10), upregulated in tumor cell lines, is expressed in human pancreatic carcinoma, but not in non-neoplastic pancreatic tissue, suggesting a role for TMSB10 in the carcinogenesis of pancreatic carcinoma.
  • CONCLUSION: Using gene expression profiling of pancreatic cell lines we were able to identify genes differentially expressed in pancreatic adenocarcinoma, which might contribute to pancreatic cancer development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Down-Regulation. Gene Expression Profiling. Pancreatic Neoplasms / genetics. Up-Regulation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Male. Middle Aged. Pancreas / metabolism. Thymosin / genetics. Thymosin / metabolism

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  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 15983444.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 61512-21-8 / Thymosin; 87397-91-9 / thymosin beta(10)
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78. Fong D, Steurer M, Obrist P, Barbieri V, Margreiter R, Amberger A, Laimer K, Gastl G, Tzankov A, Spizzo G: Ep-CAM expression in pancreatic and ampullary carcinomas: frequency and prognostic relevance. J Clin Pathol; 2008 Jan;61(1):31-5
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  • [Title] Ep-CAM expression in pancreatic and ampullary carcinomas: frequency and prognostic relevance.
  • AIMS: Pancreatic adenocarcinoma is an aggressive gastrointestinal malignancy with only a few long-term survivors even after radical surgery.
  • Patients with ampullary cancer have a better prognosis but adjuvant therapy needs further improvement.
  • Epithelial cell adhesion molecule (Ep-CAM) is strongly expressed in a variety of epithelial cancers and represents a promising target for immunological tumour therapy.
  • Thus, the aim of this study was to investigate Ep-CAM expression and its potential prognostic impact in pancreatic and ampullary carcinomas.
  • METHODS: Ep-CAM expression was investigated retrospectively by immunohistochemistry in paraffin-embedded primary tumour tissue samples from a series of consecutive patients with pancreatic (n = 153) and ampullary cancer (n = 34).
  • RESULTS: Ep-CAM overexpression was observed in 85 of 153 pancreatic cancer specimens (56%) and in 29 of 34 ampullary cancer samples (85%).
  • However, subgroup analyses showed that Ep-CAM overexpression correlated with shorter overall survival among patients with ampullary cancer and advanced stage pancreatic cancer.
  • Furthermore, in ampullary cancer, Ep-CAM overexpression was found to correlate with tumour stage.
  • CONCLUSIONS: Ep-CAM overexpression was detectable in the majority of cases with pancreatic and ampullary cancer.
  • [MeSH-major] Ampulla of Vater. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Cell Adhesion Molecules / metabolism. Common Bile Duct Neoplasms / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16775119.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / EPCAM protein, human; 0 / Neoplasm Proteins
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79. Horwhat JD, Gerke H, Acosta RD, Pavey DA, Jowell PS: Focal or diffuse "fullness" of the pancreas on CT. Usually benign, but EUS plus/minus FNA is warranted to identify malignancy. JOP; 2009;10(1):37-42
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  • [Title] Focal or diffuse "fullness" of the pancreas on CT. Usually benign, but EUS plus/minus FNA is warranted to identify malignancy.
  • CONTEXT: The role of EUS to evaluate subtle radiographic abnormalities of the pancreas is not well defined.
  • OBJECTIVE: To assess the yield of EUS+/-FNA for focal or diffuse pancreatic enlargement/fullness seen on abdominal CT scan in the absence of discrete mass lesions.
  • PATIENTS AND INTERVENTIONS: Six hundred and 91 pancreatic EUS exams were reviewed.
  • Sixty-nine met inclusion criteria of having been performed for focal enlargement or fullness of the pancreas.
  • Known chronic pancreatitis, pancreatic calcifications, acute pancreatitis, discrete mass on imaging, pancreatic duct dilation (greater than 4 mm) and obstructive jaundice were excluded.
  • RESULTS: FNA was performed in 19/69 (27.5%) with 4 new diagnoses of pancreatic adenocarcinoma, one metastatic renal cell carcinoma, one metastatic colon cancer, one chronic pancreatitis and 12 benign results.
  • CONCLUSIONS: Pancreatic enlargement/fullness is often a benign finding related to anatomic variation, but was related to malignancy in 8.7% of our patients (6/69).
  • EUS should be strongly considered as the next step in the evaluation of patients with focal enlargement of the pancreas when clinical suspicion of malignancy exists.
  • [MeSH-major] Carcinoma / diagnosis. Pancreas / pathology. Pancreas / radiography. Pancreas / ultrasonography. Pancreatic Neoplasms / diagnosis. Tomography, X-Ray Computed / methods


80. Askari MD, Tsao MS, Schuller HM: The tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone stimulates proliferation of immortalized human pancreatic duct epithelia through beta-adrenergic transactivation of EGF receptors. J Cancer Res Clin Oncol; 2005 Oct;131(10):639-48
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  • [Title] The tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone stimulates proliferation of immortalized human pancreatic duct epithelia through beta-adrenergic transactivation of EGF receptors.
  • PURPOSE: Pancreatic ductal adenocarcinoma is an aggressive smoking-associated human cancer in both men and women.
  • Binding of NNK to these receptors stimulates proliferation of pulmonary and pancreatic adenocarcinomas cells in vitro and in hamster models.
  • The goal of this study was to elucidate the NNK effects on the signal transduction pathways downstream of both beta(1)- and beta(2)-adrenergic receptors in immortalized human pancreatic HPDE6-c7 cells.
  • METHODS: The HPDE6-c7 cells are developed from normal pancreatic duct epithelial cells which are the putative cells of origin of pancreatic ductal adenocarcinoma.
  • 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT) cell proliferation assays, Western blot and cyclic AMP assays were employed to demonstrate the effects of NNK and other beta(1)- and beta(2)-adrenergic agonists and antagonist treatments on these cells.
  • RESULTS: MTT cell proliferation assays demonstrated that NNK and the classic beta-adrenergic agonist, isoproterenol, increased cell proliferation in HPDE6-c7 cells.
  • CONCLUSION: These findings suggest that the NNK -mediated beta-adrenergic receptor transactivation of the EGFR and phosphorylation of Erk1/2 in immortalized human pancreatic duct epithelial cells as a novel mechanism might contribute to the development of tobacco-associated pancreatic carcinogenesis.
  • [MeSH-major] Carcinogens / pharmacology. Cell Proliferation / drug effects. Epithelium / drug effects. Nitrosamines / pharmacology. Receptors, Adrenergic, beta-2 / drug effects
  • [MeSH-minor] Adrenergic beta-Agonists / pharmacology. Blotting, Western. Carcinoma, Pancreatic Ductal / etiology. Cell Line, Transformed. Cyclic AMP / metabolism. Humans. Isoproterenol / pharmacology. Mitogen-Activated Protein Kinase Kinases / drug effects. Mitogen-Activated Protein Kinase Kinases / metabolism. Pancreatic Ducts / drug effects. Pancreatic Neoplasms / etiology. Phosphorylation. Receptor, Epidermal Growth Factor / drug effects. Receptor, Epidermal Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Signal Transduction / physiology. Tobacco / adverse effects. Tobacco / chemistry. Transcriptional Activation / drug effects

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  • (PMID = 16091975.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Carcinogens; 0 / Nitrosamines; 0 / Receptors, Adrenergic, beta-2; 7S395EDO61 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; E0399OZS9N / Cyclic AMP; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; L628TT009W / Isoproterenol
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81. Fu XM, Dai X, Ding J, Zhu BT: Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions. J Mol Histol; 2009 Jun;40(3):189-99
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  • [Title] Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions.
  • However, the pancreas-specific PDI homolog was previously suggested to be exclusively expressed in the pancreas (thus commonly referred to as PDIp).
  • Notably, in the digestive organs, such as the stomach and pancreas, very high levels of PDIp were selectively expressed in the digestive enzyme-secreting cells (e.g., gastric chief cells and pancreatic acinar cells).
  • In addition, high levels of PDIp expression were also detected in normal human pancreas, but its expression was mostly absent in human pancreatic duct adenocarcinoma and pancreatic cancer cell lines.
  • The absence of PDIp expression in pancreatic adenocarcinoma may serve as an additional biomarker for pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / enzymology. Pancreas / enzymology. Pancreatic Neoplasms / enzymology. Protein Disulfide-Isomerases / metabolism
  • [MeSH-minor] Animals. Blotting, Western. COS Cells. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Cell Line, Tumor. Cercopithecus aethiops. Humans. Mice. Organ Specificity. Protein Transport. Subcellular Fractions / enzymology

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  • (PMID = 19821078.001).
  • [ISSN] 1567-2387
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097109; United States / NCI NIH HHS / CA / CA97109; United States / NCRR NIH HHS / RR / P20RR021940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 5.3.4.1 / Protein Disulfide-Isomerases
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82. Shi G, Zhu L, Sun Y, Bettencourt R, Damsz B, Hruban RH, Konieczny SF: Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia. Gastroenterology; 2009 Apr;136(4):1368-78
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  • [Title] Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.
  • BACKGROUND & AIMS: Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
  • METHODS: In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.
  • RESULTS: In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.

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  • (PMID = 19249398.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK055489-10; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA124586-02; United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK055489-10; United States / NCI NIH HHS / CA / CA124586-02; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586; United States / NCI NIH HHS / CA / CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Mist1 protein, mouse; 0 / Receptors, Notch; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS182460; NLM/ PMC2845927
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83. Johnson SK, Dennis RA, Barone GW, Lamps LW, Haun RS: Differential expression of insulin-like growth factor binding protein-5 in pancreatic adenocarcinomas: identification using DNA microarray. Mol Carcinog; 2006 Nov;45(11):814-27
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  • [Title] Differential expression of insulin-like growth factor binding protein-5 in pancreatic adenocarcinomas: identification using DNA microarray.
  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by its aggressiveness and resistance to both radiation and chemotherapeutic treatment.
  • To better understand the molecular pathogenesis of pancreatic cancer, DNA array technology was employed to identify genes differentially expressed in pancreatic tumors when compared to non-malignant pancreatic tissues.
  • RNA isolated from 11 PDACs and 14 non-malignant bulk pancreatic duct specimens was used to probe Affymetrix U95A DNA arrays.
  • The majority of the 150 genes identified have not been previously reported to be differentially expressed in pancreatic tumors, although a number of the upregulated transcripts have been reported previously.
  • Immunohistochemistry was used to correlate calponin and insulin-like growth factor binding protein-5 (IGFBP-5) RNA levels with protein expression in PDACs and revealed peritumoral calponin staining in the reactive stroma and intense focal staining of islets cells expressing IGFBP-5 at the edge of tumors; thus implicating the interplay of various cell types to promote neoplastic cell growth within pancreatic carcinomas.
  • As a potential modulator of cell proliferation, the overexpression of IGFBP-5 may, therefore, play a significant role in the malignant transformation of normal pancreatic epithelial cells.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Profiling. Insulin-Like Growth Factor Binding Protein 5 / genetics. Oligonucleotide Array Sequence Analysis. Pancreatic Neoplasms / genetics

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  • (PMID = 16865675.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR-16460
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Insulin-Like Growth Factor Binding Protein 5; 0 / Microfilament Proteins; 0 / calponin
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84. Shimamura T, Royal RE, Kioi M, Nakajima A, Husain SR, Puri RK: Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma. Cancer Res; 2007 Oct 15;67(20):9903-12
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  • [Title] Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma.
  • Targeting cell surface receptors with cytotoxins or immunotoxins provides a unique opportunity for tumor therapy.
  • Here, we show the efficacy of the combination therapy of gemcitabine with an interleukin-4 (IL-4) cytotoxin composed of IL-4 and truncated Pseudomonas exotoxin in animal models of pancreatic ductal adenocarcinoma (PDA).
  • We have observed that 42 of 70 (60%) tumor samples from patients with PDA express moderate- to high-density surface IL-4 receptor (IL-4R), whereas normal pancreatic samples express no or low-density IL-4R.
  • IL-4 cytotoxin was specifically and highly cytotoxic [50% protein synthesis inhibition (IC50) ranging from >0.1 to 13 ng/mL] to six of eight pancreatic cancer cell lines, whereas no cytotoxicity (IC50>1,000 ng/mL) was observed in normal human pancreatic duct epithelium cells, fibroblasts, and human umbilical vein endothelial cells (HUVEC).
  • To confirm synergistic antitumor activity in vivo and monitor precise real-time disease progression, we used a novel metastatic and orthotopic mouse model using green fluorescent protein-transfected cancer cells and whole-body imaging system.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Deoxycytidine / analogs & derivatives. Interleukin-4 / administration & dosage. Interleukin-4 / metabolism. Leukocidins / administration & dosage. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Synergism. Green Fluorescent Proteins / genetics. Humans. Mice. Mice, Nude. Receptors, Interleukin-4 / biosynthesis. Receptors, Interleukin-4 / metabolism. Recombinant Fusion Proteins / administration & dosage. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 17942922.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Receptors, Interleukin-4; 0 / Recombinant Fusion Proteins; 0W860991D6 / Deoxycytidine; 147336-22-9 / Green Fluorescent Proteins; 207137-56-2 / Interleukin-4; B76N6SBZ8R / gemcitabine
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85. Ali CW, Kaye TF, Adamson DJ, Tait IS, Polignano FM, Highley MS: CA 19-9 and survival in advanced and unresectable pancreatic adenocarcinoma and cholangiocarcinoma. J Gastrointest Cancer; 2007;38(2-4):108-14
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  • [Title] CA 19-9 and survival in advanced and unresectable pancreatic adenocarcinoma and cholangiocarcinoma.
  • BACKGROUND: The CA 19-9 tumour marker is increasingly used to monitor response to therapy in patients with pancreatic adenocarcinoma.
  • AIM OF STUDY: To assess the utility of CA 19-9 levels in the management of patients with advanced pancreatic adenocarcinoma or cholangiocarcinoma in routine clinical practice is the aim of the study.
  • METHODS: A retrospective analysis of CA 19-9 values and survival was performed in 26 patients with pancreatic adenocarcinoma receiving gemcitabine and in 18 patients with cholangiocarcinoma.
  • RESULTS: Patients with advanced pancreatic adenocarcinoma receiving gemcitabine who experienced a decrease of > or = 20% in CA 19-9 concentration had a median survival of 13.9+ months (range 4.2-23.5) compared to 7.6+ months (range 4.0-14.7) in those without such a change (p = 0.0109).
  • CONCLUSIONS: The CA 19-9 concentration has a valuable role in predicting outcome in patients with pancreatic adenocarcinoma and cholangiocarcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Bile Duct Neoplasms / mortality. CA-19-9 Antigen / blood. Cholangiocarcinoma / mortality. Pancreatic Neoplasms / mortality

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  • (PMID = 19089662.001).
  • [ISSN] 1941-6628
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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86. Price L, Kozarek R, Agoff N: Squamous cell carcinoma arising within a choledochal cyst. Dig Dis Sci; 2008 Oct;53(10):2822-5
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  • [Title] Squamous cell carcinoma arising within a choledochal cyst.
  • Most commonly reported malignancies include cholangiocarcinoma, adenocarcinoma, and gallbladder cancer.
  • Endoscopic retrograde cholangiopancreatography and direct cholangioscopy revealed a mass at the biliary bifurcation, a 4-cm choledochal cyst with multiple calculi, absence of anomalous pancreaticobiliary ductal union, and multiple calcifications in the pancreatic head.
  • Pathology demonstrated a synchronous choledochal cyst and squamous cell carcinoma, an infrequently reported phenomenon.
  • We report the associated rare finding of chronic calcific pancreatitis, without anomaly of the pancreatic biliary junction.
  • [MeSH-major] Bile Duct Neoplasms / etiology. Carcinoma, Squamous Cell / etiology. Choledochal Cyst / complications

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  • (PMID = 18274902.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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87. Tischoff I, Wittekind C, Tannapfel A: Role of epigenetic alterations in cholangiocarcinoma. J Hepatobiliary Pancreat Surg; 2006;13(4):274-9
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  • [MeSH-major] Bile Duct Neoplasms / genetics. Bile Ducts, Intrahepatic. Cholangiocarcinoma / genetics. Epigenesis, Genetic
  • [MeSH-minor] Adenocarcinoma / genetics. Apoptosis / genetics. Bile Ducts, Extrahepatic / pathology. Cell Adhesion / physiology. Cell Proliferation. Cell Transformation, Neoplastic / genetics. CpG Islands / genetics. DNA Methylation. DNA Repair / physiology. Genes, Tumor Suppressor / physiology. Humans

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  • (PMID = 16858537.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 68
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88. Tajiri T, Tate G, Inagaki T, Kunimura T, Inoue K, Mitsuya T, Yoshiba M, Morohoshi T: Intraductal tubular neoplasms of the pancreas: histogenesis and differentiation. Pancreas; 2005 Mar;30(2):115-21
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  • [Title] Intraductal tubular neoplasms of the pancreas: histogenesis and differentiation.
  • OBJECTIVES: Intraductal neoplasms of the pancreas are generally referred to as intraductal papillary mucin-producing neoplasms (IPMNs), according to the WHO classification system.
  • Cuboidal tumor cells in ITC resembled normal pancreatic duct epithelia, and the characteristic growth pattern of ITC replaced that of normal pancreatic duct epithelium.
  • Immunohistochemically, ITC cells were positive for MUC-1 on the apical side of the cell membrane.
  • In contrast to ITC cells, IPMC cells were negative for MUC-1, and ductal adenocarcinoma cells were strongly positive for MUC-1, as was the stroma around the cancer.
  • Interestingly, localization of MUC-1 and DUPAN-2 staining in ITC cells was similar to that in normal pancreatic ductules.
  • CONCLUSION: Based on our histologic and immunohistochemical findings, the intraductal pancreatic neoplasm (IPN) can be classified into 2 groups: IPN with gastrointestinal differentiation and IPN with pancreatic duct differentiation.
  • Our present data indicated that ITC cells may arise directly from duct epithelia without progression and possessed pancreatic duct differentiation.
  • On the basis of our data, we suggest that classification of pancreatic neoplasms in the WHO and The Armed Forces Institute of Pathology (AFIP) systems should be reconsidered.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Mucinous / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Renal Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 15714133.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mucins
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89. Lipsett MA, Castellarin ML, Rosenberg L: Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation. Pancreas; 2007 May;34(4):452-7
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  • [Title] Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation.
  • OBJECTIVES: The plasticity of pancreatic tissue is demonstrated in many pancreatic diseases.
  • It has previously been shown that pancreatic islet-to-duct transformation and acinoductal metaplasia have been associated with both pancreatic regeneration and adenocarcinoma in various in vivo and in vitro settings.
  • Understanding this inherent morphogenetic plasticity of the adult pancreas could lead to new therapeutic approaches to pancreatic disease.
  • Tissue samples were then analyzed for amylase, cytokeratin 19, pancreas duodenum homeobox 1, and endocrine hormone immunoreactivity as well as dithizione positivity.
  • Addition of INGAP led to an approximately 18-fold increase in pancreas duodenum homeobox 1 immunoreactivity, although without an observed increase in insulin production as measured by dithizone positivity.
  • CONCLUSIONS: We have developed a novel in vitro model of adult human acinoductal metaplasia that will aid not only in developing new methods of expanding beta-cell mass but also provide insights into pancreatic carcinogenesis.
  • [MeSH-major] Cell Differentiation. Islets of Langerhans / pathology. Pancreatic Ducts / pathology. Regeneration
  • [MeSH-minor] Adult. Amylases / metabolism. C-Peptide / metabolism. Cell Proliferation. Cells, Cultured. Cytokines / pharmacology. Gastrins / pharmacology. Hepatocyte Growth Factor / pharmacology. Homeodomain Proteins / biosynthesis. Humans. Insulin-Secreting Cells / pathology. Keratin-19 / metabolism. Metaplasia. Pancreas / pathology. Pancreas / physiopathology. Peptide Fragments / pharmacology. Phenotype. Time Factors. Trans-Activators / biosynthesis. Up-Regulation

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  • (PMID = 17446845.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C-Peptide; 0 / Cytokines; 0 / Gastrins; 0 / Homeodomain Proteins; 0 / INGAP peptide; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 67256-21-7 / Hepatocyte Growth Factor; EC 3.2.1.- / Amylases
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90. Schönleben F, Qiu W, Allendorf JD, Chabot JA, Remotti HE, Su GH: Molecular analysis of PIK3CA, BRAF, and RAS oncogenes in periampullary and ampullary adenomas and carcinomas. J Gastrointest Surg; 2009 Aug;13(8):1510-6
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  • While oncogenic BRAF contributes to the tumorigenesis of both pancreatic ductal adenocarcinoma and intraductal papillary mucinous neoplasms/carcinomas (IPMN/IPMC), PIK3CA mutations were only detected in IPMN/IPMC.

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  • (PMID = 19440799.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109525-05; United States / NCI NIH HHS / CA / R21 CA127701; United States / NCI NIH HHS / CA / CA127701-01A2; United States / NCI NIH HHS / CA / R01CA109525; United States / NCI NIH HHS / CA / R01 CA109525; United States / NCI NIH HHS / CA / CA109525-05; United States / NCI NIH HHS / CA / R21 CA127701-01A2; United States / NCI NIH HHS / CA / R21CA127701
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS164917; NLM/ PMC3915027
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91. Fasanella KE, McGrath K: Cystic lesions and intraductal neoplasms of the pancreas. Best Pract Res Clin Gastroenterol; 2009;23(1):35-48
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  • [Title] Cystic lesions and intraductal neoplasms of the pancreas.
  • Pancreatic cystic lesions are being detected more frequently given increased use of cross-sectional imaging modalities.
  • These include main duct diameter > or = 10 mm, a branch duct size > or = 3 cm, presence of a mural nodule, or cytology suspicious for malignancy.
  • Branch duct IPMN is less aggressive that the main duct variety, and may be conservatively followed.
  • Despite generalized guidelines, decisions regarding management of pancreatic cysts should be individualized, accounting for the malignant risk of the lesion and the surgical risk of the patient.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma, Mucinous / pathology. Carcinoma, Papillary / pathology. Cell Transformation, Neoplastic / pathology. Cholangiopancreatography, Magnetic Resonance. Cystadenoma, Mucinous / pathology. Cystadenoma, Serous / pathology. Endosonography. Humans. Pancreatic Pseudocyst / pathology. Tomography, X-Ray Computed

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  • (PMID = 19258185.001).
  • [ISSN] 1532-1916
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 66
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92. Bickenbach K, Galka E, Roggin KK: Molecular mechanisms of cholangiocarcinogenesis: are biliary intraepithelial neoplasia and intraductal papillary neoplasms of the bile duct precursors to cholangiocarcinoma? Surg Oncol Clin N Am; 2009 Apr;18(2):215-24, vii
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  • [Title] Molecular mechanisms of cholangiocarcinogenesis: are biliary intraepithelial neoplasia and intraductal papillary neoplasms of the bile duct precursors to cholangiocarcinoma?
  • Although the key steps of cholangiocarcinogenesis remain unknown, it has been hypothesized that CC may develop through two key premalignant precursor lesions: biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of the bile duct (IPNB).
  • These lesions probably are analogous to pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm, respectively.
  • It highlights the genetic mutations that alter cellular proliferation, tumor suppression, and impairment of critical mucinous, cell-adhesion, and matrix proteins.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic / pathology. Cholangiocarcinoma / pathology. Precancerous Conditions / pathology

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  • (PMID = 19306808.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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93. Morton JP, Lewis BC: Shh signaling and pancreatic cancer: implications for therapy? Cell Cycle; 2007 Jul 1;6(13):1553-7
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  • [Title] Shh signaling and pancreatic cancer: implications for therapy?
  • Hedgehog signaling has been implicated in the development of several human cancers, including small cell lung carcinomas, medulloblastomas, basal cell carcinomas, and digestive tract tumors.
  • Elevated levels of pathway components are observed in pancreatic ductal adenocarcinoma (PDAC) precursor lesions, and these levels increase further as lesions progress to more advanced stages.
  • Yet the mechanisms by which hedgehog signaling contributes to pancreatic tumorigenesis were poorly understood.
  • We recently published results showing that activated hedgehog signaling enhances the proliferation and survival of pancreatic duct epithelial cells, the presumptive target cells for PDAC development.
  • We also demonstrated that sonic hedgehog (Shh) expression, in cooperation with loss of the Trp53 and Ink4a/Arf tumor suppressor loci, was sufficient to initiate the formation of early pancreatic lesions.
  • Furthermore, Shh signaling enhanced K-Ras-mediated pancreatic tumorigenesis and reduced the dependence of tumor cells on the sustained activation of Ras-stimulated signaling pathways.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / therapy. Hedgehog Proteins / physiology. Pancreatic Neoplasms / therapy

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  • (PMID = 17611415.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Hedgehog Proteins; 0 / SHH protein, human
  • [Number-of-references] 41
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94. Demeter I, Hegyesi O, Nagy AK, Case MR, Steward MC, Varga G, Burghardt B: Bicarbonate transport by the human pancreatic ductal cell line HPAF. Pancreas; 2009 Nov;38(8):913-20
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  • [Title] Bicarbonate transport by the human pancreatic ductal cell line HPAF.
  • OBJECTIVES: The human pancreatic duct cell line, HPAF, has been shown previously to secrete Cl(-) in response to Ca(2+)-mobilizing stimuli.
  • [MeSH-minor] 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / analogs & derivatives. 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Adenosine Triphosphate / pharmacology. Amiloride / analogs & derivatives. Amiloride / pharmacology. Biological Transport / drug effects. Bumetanide / pharmacology. Cell Line, Tumor. Chlorides / metabolism. Cytophotometry. Fluoresceins / chemistry. Humans. Hydrogen-Ion Concentration. Intracellular Space / chemistry. Ion Transport / drug effects. Membrane Potentials / drug effects. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology. Pancreatic Ducts / physiopathology. Sodium Potassium Chloride Symporter Inhibitors / pharmacology. Sodium-Potassium-Chloride Symporters / metabolism. Solute Carrier Family 12, Member 2

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  • (PMID = 19745779.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bicarbonates; 0 / Chlorides; 0 / Fluoresceins; 0 / SLC12A2 protein, human; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / Sodium-Potassium-Chloride Symporters; 0 / Solute Carrier Family 12, Member 2; 0Y2S3XUQ5H / Bumetanide; 1154-25-2 / ethylisopropylamiloride; 61481-03-6 / dihydro-DIDS; 7DZO8EB0Z3 / Amiloride; 85138-49-4 / 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein; 8L70Q75FXE / Adenosine Triphosphate; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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95. Kubota K, Kakuta Y, Inayama Y, Yoneda M, Abe Y, Inamori M, Kirikoshi H, Saito S, Nakajima A, Sugimori K, Matuo K, Kazunaga T, Shimada H: Clinicopathologic study of resected cases of primary carcinoma of the cystic duct. Hepatogastroenterology; 2008 Jul-Aug;55(85):1174-8
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  • [Title] Clinicopathologic study of resected cases of primary carcinoma of the cystic duct.
  • BACKGROUND/AIMS: There have been few reports of primary carcinoma of the cystic duct (CCD) included in advanced cases.
  • METHODOLOGY: Six cases of CCD were diagnosed in which the main carcinomatous component arose from the cystic bile duct, even if these carcinomas were accompanied by invasion beyond the cystic duct.
  • Histopathologic findings (i.e., H.E. staining and cell proliferating potency assessed by ki-67 staining) were compared between the main lesion and invasive lesion of the CCD.
  • Direct cholangiography demonstrated unilateral obstruction of the common bile duct in 4 out of the 6 cases.
  • Histopathological study revealed papillary and/or well differentiated adenocarcinoma in the cases where the lesion predominantly involved the cystic duct, whereas those lesions which extended beyond the cystic duct were composed of moderate and/or poorly differentiated tubular adenocarcinoma.
  • CONCLUSIONS: CCD showed the hepatic hilum and/or confluence pattern of invasion when the tumor extended beyond the cystic duct.
  • CCD extending beyond the cystic duct was associated with more aggressive characteristics of the tumors, with perineural infiltration and histopathologic features resembling those of pancreatic cancer.
  • It is concluded that CCDs extending beyond the cystic duct are more aggressive and associated with a poorer prognosis.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Duct Neoplasms / surgery. Carcinoma / pathology. Carcinoma / surgery. Cystic Duct

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  • (PMID = 18795652.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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96. Zhu L, Shi G, Schmidt CM, Hruban RH, Konieczny SF: Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am J Pathol; 2007 Jul;171(1):263-73
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  • [Title] Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
  • A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
  • PanINs are thought to initiate in the small ducts of the pancreas through activating mutations in the KRAS proto-oncogene.
  • What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation.
  • To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease.
  • In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells.

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  • (PMID = 17591971.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK55489; United States / NCI NIH HHS / CA / P50 CA62924; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Erbb2ip protein, mouse; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Isgf3g protein, mouse; 0 / Receptors, Notch
  • [Other-IDs] NLM/ PMC1941579
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97. Löhr M, Klöppel G, Maisonneuve P, Lowenfels AB, Lüttges J: Frequency of K-ras mutations in pancreatic intraductal neoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta-analysis. Neoplasia; 2005 Jan;7(1):17-23
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  • [Title] Frequency of K-ras mutations in pancreatic intraductal neoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta-analysis.
  • Molecular analyses have demonstrated mutations in the K-ras gene at codon 12 in the majority of pancreatic ductal adenocarcinomas (PDACs).
  • In order to determine whether the K-ras mutation rate increases parallel to the grade of dysplasia in duct lesions, we performed a meta-analysis of the studies published between 1988 and 2003 that provide information on K-ras mutations in hyperplastic and dysplastic duct lesions in the pancreas.
  • The described duct lesions were reclassified according to the nomenclature for pancreatic intraepithelial neoplasia (PanIN), and the molecular methods for detecting K-ras were reviewed.
  • The incidence of K-ras mutations in PanIN lesions associated with chronic pancreatitis (CP) or normal pancreas was low (around 10%).
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Genes, ras / genetics. Mutation / genetics. Pancreatic Ducts / pathology. Pancreatic Neoplasms / genetics. Pancreatitis / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Humans

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  • (PMID = 15720814.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1490318
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98. Schmidt CM, White PB, Waters JA, Yiannoutsos CT, Cummings OW, Baker M, Howard TJ, Zyromski NJ, Nakeeb A, DeWitt JM, Akisik FM, Sherman S, Pitt HA, Lillemoe KD: Intraductal papillary mucinous neoplasms: predictors of malignant and invasive pathology. Ann Surg; 2007 Oct;246(4):644-51; discussion 651-4
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  • IPMN type and main pancreatic duct diameter were significant predictors of malignant IPMN (P<0.001).
  • CONCLUSIONS: To lower the rate of invasive pathology, surgery should be recommended for fit patients with main-duct IPMN and for branch-duct IPMN with mural nodularity or positive cytology irrespective of location, distribution, or size.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / pathology. Cohort Studies. Female. Forecasting. Humans. Laparoscopy. Male. Middle Aged. Neoplasm Invasiveness. Pancreatectomy. Pancreaticoduodenectomy. Prospective Studies. Retrospective Studies. Survival Rate

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  • (PMID = 17893501.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R03CA112629-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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99. Kendrick ML, Cusati D: Total laparoscopic pancreaticoduodenectomy: feasibility and outcome in an early experience. Arch Surg; 2010 Jan;145(1):19-23
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  • The pancreaticojejunostomy consisted of a duct-to-mucosa anastomosis with interrupted suture.
  • Diagnosis was pancreatic adenocarcinoma (n = 31), intraductal papillary mucinous neoplasm (n = 12), periampullary adenocarcinoma (n = 8), neuroendocrine tumor (n = 4), chronic pancreatitis (n = 3), cholangiocarcinoma (n = 1), metastatic renal cell carcinoma (n = 1), cystadenoma (n = 1), and duodenal adenoma (n = 1).
  • Perioperative morbidity occurred in 26 patients and included pancreatic fistula (n = 11), delayed gastric emptying (n = 9), bleeding (n = 5), and deep vein thrombosis (n = 2).
  • [MeSH-major] Pancreatic Diseases / surgery. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods

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  • (PMID = 20083750.001).
  • [ISSN] 1538-3644
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. Bogoevski D, Chayeb H, Cataldegirmen G, Schurr PG, Kaifi JT, Mann O, Yekebas EF, Izbicki JR: Nodal microinvolvement in patients with carcinoma of the papilla of vater receiving no adjuvant chemotherapy. J Gastrointest Surg; 2008 Nov;12(11):1830-7; discussion 1837-8
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  • METHODS: From 1993 to 2003 at the University Clinic Hamburg, 777 patients were operated upon pancreatic and periampullary carcinomas.
  • The vast majority of patients were operated upon pancreatic ductal adenocarcinoma (n = 566, 73%), followed by carcinomas of the papilla of Vater (n = 112, 14%), pancreatic neuroendocrine carcinomas (n = 39, 5%), intraductal papillary mucinous neoplasms (n = 33, 4%), and distal bile duct carcinomas (n = 27, 3%).
  • Fresh-frozen tissue sections from 169 lymph nodes (LNs) classified as tumor free by routine histopathology from 57 patients with R0 resected carcinoma of the papilla of Vater who had been spared from adjuvant chemotherapy were immunohistochemically (IHC) examined, using a sensitive IHC assay with the anti-epithelial monoclonal antibody Ber-EP4 for tumor cell detection.
  • CONCLUSIONS: The influence of occult tumor cell dissemination in LNs of patients with histologically proven carcinoma of the papilla of Vater supports the need for further tumor staging through immunohistochemistry.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / surgery. Ampulla of Vater / pathology. Common Bile Duct Neoplasms / pathology. Common Bile Duct Neoplasms / surgery. Lymph Nodes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Chemotherapy, Adjuvant. Cohort Studies. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / mortality. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Statistics, Nonparametric. Survival Analysis. Treatment Outcome

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  • (PMID = 18791769.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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